ArticleAmerican journal of physiology. Renal physiology2014
Iodinated contrast media cause direct tubular cell damage, leading to oxidative stress, low nitric oxide, and impairment of tubuloglomerular feedback.
Article in American journal of physiology. Renal physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.
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Who cites it
31 citing papers in PubMed, 1 synthesis or guideline pooled it, 70 citations in OpenAlex.
- Efficacy of Chronic Use of Sodium-Glucose Co-transporter 2 Inhibitors on the Prevention of Contrast-Induced Acute Kidney Injury in Patients with Type 2 Diabetes Mellitus Following Coronary Procedures: A Systematic Review and Meta-Analysis.American journal of cardiovascular drugs : drugs, devices, and other interventions · 2025Pooled it
- Inorganic nitrate benefits contrast-induced nephropathy after coronary angiography for acute coronary syndromes: the NITRATE-CIN trial.European heart journal · 2024Trial
- Assessment of an advanced virtual monoenergetic reconstruction technique in cerebral and cervical angiography with third-generation dual-source CT: Feasibility of using low-concentration contrast medium.European radiology · 2018Trial
- Iomeprol X-ray contrast media alter conformation and affinity of the ATP binding pocket of actin.Biophysical journal · 2026Article
- Renal Resistive Index as a Novel Predictor of Contrast-Induced Acute Kidney Injury in Cirrhosis.Cureus · 2026Article
- Contrast Media in Hospitalized Patients with Acute Kidney Injury: Renal and Clinical Outcomes.American journal of nephrology · 2026Article
- Experimental study of intravoxel incoherent motion diffusion imaging combined with ultrasound renal resistance index in contrast-induced nephropathy.BMC nephrology · 2025Article
- Contrast-induced acute kidney injury: a review of definition, pathogenesis, risk factors, prevention and treatment.BMC nephrology · 2024Review
- Incomplete Recovery from the Radiocontrast-Induced Dysregulated Cell Cycle, Adhesion, and Fibrogenesis in Renal Tubular Cells after Radiocontrast (Iohexol) Removal.International journal of molecular sciences · 2023Article
- Interleukin-18 and Gelsolin Are Associated with Acute Kidney Disease after Cardiac Catheterization.Biomolecules · 2023Article
- Renal resistance index independently predicts worsening of renal function after coronary angiography.The international journal of cardiovascular imaging · 2023Article
- Statin Use Influence on the Occurrence of Acute Kidney Injury in Patients with Peripheral Arterial Disease.Journal of atherosclerosis and thrombosis · 2022Article
- Contrast-Associated Acute Kidney Injury After Endovascular Therapy for Acute Ischemic Stroke: A Meta-Analysis.Stroke (Hoboken, N.J.) · 2022Article
- Circular RNAs in Acute Kidney Injury: Roles in Pathophysiology and Implications for Clinical Management.International journal of molecular sciences · 2022Review
- The Pathophysiology and the Management of Radiocontrast-Induced Nephropathy.Diagnostics (Basel, Switzerland) · 2022Review
- MG53 protects against contrast-induced acute kidney injury by reducing cell membrane damage and apoptosis.Acta pharmacologica Sinica · 2020Article
- Limb ischemic preconditioning ameliorates renal microcirculation through activation of PI3K/Akt/eNOS signaling pathway after acute kidney injury.European journal of medical research · 2020Article
- Evaluation of iodine contrast-induced acute kidney injury via different injection routes using BOLD-MRI.Renal failure · 2019Article
- "I don't get no respect": the role of chloride in acute kidney injury.American journal of physiology. Renal physiology · 2019Review
- Rate and risk factors for AKI after CT scans in a cancer cohort .Clinical nephrology · 2019Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
Abstract
Iodinated contrast media (CM) have adverse effects that may result in contrast-induced acute kidney injury. Oxidative stress is believed to play a role in CM-induced kidney injury. We test the hypothesis that oxidative stress and reduced nitric oxide in tubules are consequences of CM-induced direct cell damage and that increased local oxidative stress may increase tubuloglomerular feedback. Rat thick ascending limbs (TAL) were isolated and perfused. Superoxide and nitric oxide were quantified using fluorescence techniques. Cell death rate was estimated using propidium iodide and trypan blue. The function of macula densa and tubuloglomerular feedback responsiveness were measured in isolated, perfused juxtaglomerular apparatuses (JGA) of rabbits. The expression of genes related to oxidative stress and the activity of superoxide dismutase (SOD) were investigated in the renal medulla of rats that received CM. CM increased superoxide concentration and reduced nitric oxide bioavailability in TAL. Propidium iodide fluorescence and trypan blue uptake increased more in CM-perfused TAL than in controls, indicating increased rate of cell death. There were no marked acute changes in the expression of genes related to oxidative stress in medullary segments of Henle's loop. SOD activity did not differ between CM and control groups. The tubuloglomerular feedback in isolated JGA was increased by CM. Tubular cell damage and accompanying oxidative stress in our model are consequences of CM-induced direct cell damage, which also modifies the tubulovascular interaction at the macula densa, and may therefore contribute to disturbances of renal perfusion and filtration.
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